The objective of this proposal is to understand the behavioral significance of functional modifications produced in an identified neural circuit in the abdominal ganglion of the marine mullusk, Aplysia. This circuit consists of an interneuron (L10) and four of its endogenously active follower cells (the left upper quadrant bursting cells). Earlier neurophysiological studies by the author and others in the isolated ganglion have described (1) the diphasic nature of the parallel inhibitory synaptic connections between the interneuron and the LUQ cells, and (2) functional modifications of the endogenous bursting rhythm produced by contingent firing of the interneuron. The first aim of the present proposal is to bring together these two lines of research by analyzing the presynaptic and postsynaptic mechanisms that underly the functional modifications of the bursting rhythm. This will be accomplished by means of pharmacological and electrophysiological techniques in the isolated ganglion that selectively block or selectively mimic the two components of the diphasic IPSP. The significance of this part of the proposed research is that it can elucidate the cellular mechanism of a relatively unexplored type of neural plasticity that may be of general interest. Plasticity of endogenous pacemaker properties of nerve cells can be viewed as a neural analog of an operant conditioning paradigm. The second aim of this proposal is to extend the work in the isolated ganglion to the intact animal in order to analyze the behavioral function of the central neural circuit. This will be accomplished by means of a combination of anatomical, electrophysiological and behavioral techniques in a semi- intact preparation and then in the intact animal. The significance of this part of the proposed research is that it can specify the behavioral function of a well-documented neural circuit and might, therefore, be used to investigate the behavioral consequence of the short-term plastic changes in the pacemaker properties of these cells.